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Many dogs display coprophagic behaviour. Helminth eggs can passively pass the dog's digestive tract and this may result in a false positive diagnosis of infection with gastrointestinal helminth parasites. For a period of one year, faecal samples of dogs were examined monthly using the Centrifugal Sedimentation Flotation (CSF) technique with a sugar flotation solution (s.g. 1.27-1.30 g/cm(3)). If a sample tested positive for canine helminth eggs, the owner was asked to submit another sample after preventing the dog from eating faeces for 3 days. If the second sample again tested positive for the same type of helminth egg, the dog was considered to have a patent infection. If the second sample tested negative, the first sample was considered a false positive due to coprophagy. The focus of this study was on dogs shedding Toxocara eggs. At the first examination, 246 samples (out of 308 samples testing positive for canine-specific helminth eggs) tested positive for Toxocara spp. Of these, 120 (49%) tested negative at the second examination. Coprophagic behaviour was recognized by 261 of the 564 owners that answered the accompanying questionnaire. This concerned 391 dogs. Coproscopical examination also provided proof of coprophagy (e.g. oocysts of Eimeria spp. or non-dog typical helminth eggs) in dogs belonging to owners that did not report coprophagic behaviour in their dogs. Results indicate that coprophagy in dogs may result in an overestimation of the prevalence of patent helminth infections and that dogs may serve as a transport host for helminth eggs., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Coprophagous activity is normal among broiler chickens. The purpose of this study was to compare an individually housed chick model (where bird-to-bird coprophagia was prevented) to a group-housed chick model (where bird-to-bird coprophagia was allowed) for determining estimates of the number of Campylobacter jejuni RM1221 necessary to colonize 50% of broiler chicks inoculated (colonization dose 50% or CD(50)). Campylobacter jejuni RM1221 was orally administered in measured doses to newly hatched chicks. The chicks were housed either individually in cages designed to minimize coprophagous activity or in isolation units containing groups of birds where coprophagia was allowed. The birds were killed and analyzed for Campylobacter in the ceca on d 7 postinoculation. The CD(50) was calculated, and results from the 2 models were compared. Elimination of transmission of Campylobacter, through coprophagia or other means, led to a more clear determination of the estimated CD(50) of about 524 cfu of C. jejuni RM1221 as demonstrated in the individually housed chick model. Bayesian inference based on the beta-Poisson statistical modeling procedures were found to be superior to standard single-hit dose-response modeling for estimation of the CD(50). This study demonstrated that the individual bird challenge model is superior to the group challenge model for trials designed to determine colonization dose.

Five to 20 mg of saponins obtained from alfalfa tops or roots were introduced intragastrically in rats also receiving oral and intravenous ring-labeled cholesterol. The saponins were tested before and after partial acid hydrolysis. Absorption of cholesterol was determined by estimation of fecal sterols and by a dual isotope technique involving assay of plasma radioactivity. Alfalfa top saponins (nonhydrolyzed) reduced absorption of cholesterol. Acid hydrolysis of alfalfa top or root saponins enhanced their ability to inhibit cholesterol absorption.

Several methods for measuring cholesterol absorption in the rat have been compared. After administration of an oral dose of labeled cholesterol ((14)C or (3)H) and an intravenous dose of colloidal labeled cholesterol ((3)H or (14)C) the ratio of the two labels in plasma or whole blood 48 hr or more after dosing compared closely to the ratio of areas under the respective specific activity-time curves. The area ratio method is independent of a time lag between the appearance of oral and intravenous label in the bloodstream. Both measures of cholesterol absorption agree fairly well with a method based on measuring the unabsorbed dietary cholesterol in a pooled fecal sample. The plasma isotope ratio method gave more reproducible results than the fecal collection method when the measurement was repeated in the same animals 5 days after the first measurement. Cholesterol absorption was overestimated by the use of Tween 20-solubilized labeled cholesterol for the intravenous dose. The plasma disappearance curves of injected labeled colloidal cholesterol and cholesterol-labeled chylomicrons infused intravenously over a 3.5-hr period in the same animal coincided within experimental error from the first day until 75 days after injection. The plasma isotope ratio method for cholesterol absorption gave the same results in rats practicing coprophagy as in those in which this practice was prevented. The addition of sulfaguanidine to the diet lowered cholesterol absorption as measured by the plasma isotope ratio to the same degree as that measured by the fecal collection method.

When a diet containing raw soybean was fed to rats, there was an increase in the synthesis of pancreatic protein, presumably exocrine protein, as evidenced by an increased uptake of [35S]cystine. There was also an increased transsulfuration of methionine sulfur as indicated by labeled sulfur transformation from methionine to cystine. This same pattern of events was produced in rats receiving a casein-containing diet when 50 mg of crystalline trypsin inhibitor was administered by gavage. However, if coprophagy was prevented, the increased uptake of [35S]cystine and [35S]methionine transsulfuration under both dietary conditions was blocked. It was found that prevention of coprophagy was without effect upon these two processes if supplementary dietary cystine was provided or if a dietary protein source with adequate cystine, i.e., heat-treated soybean, was provided. It was concluded that by practicing coprophagy, sufficient fecal cystine was being returned to the upper intestinal tract to permit some synthesis of pancreatic exocrine protein and with this stimulation of synthesis, transulfuration could proceed. This assumes that the biosynthesis of cystine is dependent upon the availability of sufficient cystine to permit active protein synthesis. In another situation where cystine requirement is high, namely, the rapidly growing rat, a limited amount of cystine was fed by providing a 12% casein diet. Either supplementary cystine or methionine was provided and it was found that both amino acids gave optimal growth in conventional rats, but when coprophagy was prevented, optimal growth was achieved only with the cystine-supplemented diet.

Effects of ascorbic acid ingestion on the severity of vitamin B-12 deficiency were investigated by feeding weanling rats experimental diets containing 0-100 micrograms of vitamin B-12 activity per kg of diet, with or without 6.0 mg of ascorbic acid per ml supplied in drinking water for 15 wk. This daily consumption of up to 150 mg of ascorbic acid did not impair growth, but did result in significantly higher concentrations of ascorbic acid in plasma, liver, adrenal glands and feces. When rats were fed diets deficient or marginally deficient in vitamin B-12, liver concentrations of vitamin B-12 were markedly lower than in liver of rats fed adequate vitamin B-12. Ascorbic acid ingestion raised values significantly in the vitamin B-12-deficient diet group. Urinary methylmalonic acid was significantly elevated in the deficient rats. However, it was significantly reduced to more normal values by ascorbic acid in rats with both low and marginal vitamin B-12 status, as defined by dietary and liver concentrations of vitamin B-12 activity. Although coprophagy was not prevented, rats showed no increased consumption of feces with the higher ascorbic acid content. Thus, the results of this research indicate that vitamin C ingestion partially protects rats from vitamin B-12 deficiency.